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Ascites tumor cells

The kind of detailed quantitative information the method can yield is well illustrated by the determination of the total dry weight of individual ascites tumor cells, the volume of each cell being less than 4 X 10" 9 cc. The total dry weight, mc, of a cell is given by... [Pg.299]

Ascites tumor cells, determination of dry weight of individual, 299, 300 Atomic absorption coefficient, 15 Atomic energy program, use of x-ray absorptiometry in, 96 Atomic number, significance proved by Moseley, 28, 29... [Pg.340]

Osterreich, S., Schunck, H., Benndorf, R., Bielka, H. (1991). Cisplatin induces the small heat shock protein hsp25 and thermotolerance in Ehrlich ascites tumor cells. Biochem. Biophys. Res. Comm. 180,243-248. [Pg.458]

Iliakis G. 1984. The mutagenicity of alpha particles in ehrlich ascites tumor cells. Radiat Res 99 52-58. [Pg.243]

ATPase activity of P-glycoprotein related to emergence of drug resistance in Ehrlich ascites tumor cell lines, Biochim. Biophys. Acta 1997,... [Pg.492]

Panniers, R., and Henshaw, E. C. (1983). A GDP/GTP exchange factor essential for eukaryotic initiation factor 2 cycling in Ehrlich ascites tumor cells and its regulation by eukaryotic initiation factor 2 phosphorylation. J. Biol. Chem. 258, 7928—7934. [Pg.50]

Xanthothricin 308 stimulated oxidation of NADH and NAD-linked substrates by rat liver mitochondria, yeast mitochondria, and Ehrlich ascites tumor cells (74MI1, 74MI3). It also stimulated mitochondrial oxidation of succinate, pyruvate, or malate. The antibiotic xanthothricin was obtained... [Pg.261]

B. Chance, D. Garfinkel, J. Higgins, and B. Hess, Metabolic control mechanisms A solution for the equations representing interaction between glycolysis and respiration in ascites tumor cells. [Pg.238]

Agranofl, B. W., Hajra, A. K. The acyl dihydroxyacetone phosphate pathway for glycerolipid biosynthesis in mouse liver and Ehrlich ascites tumor cells. Proc. Natl. Acad. Sci. U.S. 68, 411-415 (1971). [Pg.68]

A protein highly homologous to the S100 proteins has been isolated from Ehrlich ascites tumor cells it has subsequently been shown to be nearly identical with human calcyclin. The fluorescence intensity from the three tyrosine residues is enhanced on the binding of Ca2+.(l58)... [Pg.35]

Fetner has also demonstrated chromatid breaks in a human tissue-culture cell line exposed to ozone at 8 ppm for 5 min. Other tissue-culture studies include that of Sachsenmaier et who noted tetraploidy and other chromosomal abnormalities in embryonic chick fibroblasts exposed to ozone and a decrease in transplantability of mouse ascites tumor cells. In addition, Pace et demonstrated an interference by ozone with mitotic activity in two tissue-culture cell lines. More recently, Booher et al. reported that lung cells exposed in culture to ozone concentrations as low as 0.3 ppm demonstrated an inhibition in growth that was proportional to the ozone concentration. [Pg.364]

In different organs of the rat [128], Ehrlich ascites tumor cells [144], trout testis [127], calf thymus [145], and carp testis [146], H4 is modified mainly as the N -dimethyllysine, while H3 is modified as N -monomethyllysine, N -dimethylly-sine and N -trimethyllysine with the N -dimethyllysine predominating. Pea seedling H4 is not methylated and H3 exits as N -mono- and N -dimethyllysine with N -trimethyllysine not being detectable [147,148]. [Pg.218]

The temporal sequence of H3 and H4 methylation after synthesis has been examined in Ehrlich ascites tumor cells [144] and trout testis [149]. Methylation lagged histone synthesis, and the histone was methylated after being bound to DNA. H4 methylation follows the stepwise acetylations and deacetylations [149]. It was suggested that methylation was involved in final arrangement of H3 and H4 on newly replicated DNA [144] and might be involved in histone interactions with other proteins such as histone kinases [149]. [Pg.218]

Gregory, R.I. et al. (2002) Inhibition of histone deacetylases alters allelic chromatin conformation at the imprinted U2afl-rsl locus in mouse embryonic stem cells. J. Biol. Chem. 277, 11728-11734. Thomas, G., Lange, H.W., and Hempel, K. (1975) Kinetics of histone methylation in vivo and its relation to the cell cycle in Ehrlich ascites tumor cells. Eur. J. Biochem. 51, 609-615. [Pg.305]

Woerdenbag HI, Moskal TA, Pras N, Malingre TM, El-Feraly FS, Kampinga HH, Konings AWT. (1993) Cytotoxicity of artemisinin-related endoperox-ides to Ehrlich ascites tumor cells. J Nat Prod 56 849-856. [Pg.333]

Not only have animals or isolated organs of animals been used to perform pharmacological studies, but also cells in culture. In a study done by Prof. Yamasaki25 at the University of Hiroshima (Figure 16.28), Ehrlich ascites tumor cells have been used to demonstrate the increase of glucose transport into the cell as a function of G115. [Pg.227]

Effect of standardized P. ginseng extract G115 on the glucose transport in Ehrlich ascites tumor cells. [Pg.229]

K. Yamasaki et al., Effects of the standardized ginseng extract G115 on the D-glucose transport by Ehrlich ascites tumor cells, Phytother. Res., 7, 200, 1993. [Pg.234]

Other pathways to better resolution and enhanced sensitivity may involve methods used in NMR studies of cellular phosphorus dynamics and humic and fulvic materials of water, soil, and sediments. These techniques include a variety of extractions, ion-pairing reagents, adsorption techniques, and lanthanide-shift reagents. For example, an extraction technique that has greatly enhanced the resolution and sensitivity of 31P FT-NMR spectra of Ehrlich ascites tumor cells (53) and HeLa cells (54) is the addition of 35% perchloric acid and removal of acid-insoluble material, followed by filtration and neutralization with K.2C03 or NaOH. [Pg.192]

It has been found that a similar type of self-regulatory active transport also operates in mammalian cells, in this case in the Ehrlich ascites tumor cell (41). These cells show an active concentrative ability for glucose at low ambient glucose concentrations. This enables the cell to... [Pg.280]

Figure 4. Accumulation of glucose by ascites tumor cells under semi-steady -... Figure 4. Accumulation of glucose by ascites tumor cells under semi-steady -...
The hexokinases from yeast or ascites tumor cells showed only a marginal preference for a-glucose. The Km values for a- and /3-glucose (58 and 66 mM for the yeast enzyme and 77 and 82 mM for the tumor enzyme) were essentially the same, and the turnover numbers were only 10-20% higher with a-glucose. [Pg.295]

Acid Complexes from Ascites Tumor Cells, Federation Proc. (1963) 22, 417. [Pg.313]

K. 5 -Nudeotidase from Ehrlich Ascites Tumor Cells. . . 348... [Pg.337]

Murray and Friedrichs (80) have obtained a 5 -nucleotidase from a particulate fraction of Ehrlich ascites tumor cells using deoxycholate. The relative rates of hydrolysis of 5 -UMP, 5 -AMP, 5 -CMP, 5 -GMP, and 5 -IMP are 129, 100, 93, 83, and 79, respectively. Adenosine and thymidine triphosphate are competitive inhibitors of 5 -AMP hydrolysis... [Pg.348]

Outline of purification scheme for UMP synthase from Ehrlich s ascites tumor cells of mice. [Pg.127]

Traub, P., Perides, G., Scherbarth, A., and Traub, U. (1985). Tenacious binding of lipids to vimentin during its isolation and purification from Ehrlich ascites tumor cells. FEBSLett. 193, 217-221. [Pg.200]

Stabilized Ehrlich ascites tumor cell membranes 411... [Pg.145]

Considerable evidence has shown that selenium can inhibit the growth of experimentally transplanted tumors (65-74) One of the principal cell lines that has been used for many of these studies has been the Ehrlich ascites tumor cell (65-68) Abdullaev et al., (65) showed that the parenteral administration of sodium selenite at a dose of 1 ug per g body weight of the host retarded the growth of this tumor cell line. Additional studies also revealed that similar quantities of jelenium inhibited the growth of Guerin carcinoma, sarcomatous M neoplasms and L-1210 leukemic cells (65, 74) ... [Pg.273]

On day zero,.mice weighing approximately 20 g were inoculated with 5 X 10 Ehrlich ascites tumor cells (EATC) SEM = standard error of the mean. All test solutions were prepared in Krebs Ringers Phosphate buffer and administered by i.p. injection on days 0, 1, 3, 5, 7, 9, 12, 15, and 18. [Pg.274]

Adapted from Poirier and Milner (69). All tumor cells were preincubated for 15 minutes in buffer in the presence or absence of selenium as sodium selenite, selenodiglutathione or dimethyl-selenide, before inoculation into Swiss mice. Each received 5 X 10 Ehrlich ascites tumor cells. Vertical means SEM not sharing a common superscript letter differ P < 0.05. [Pg.279]

Dano K. Active outward transport of daunomycin in resistant Ehrlich ascites tumor cells. Biochim Biophys Acta 1973 323 466 483. [Pg.191]

Skovsgaard T. Mechanisms of resistance to daunombicin in Ehrlich ascites tumor cells. Cancer Res 1978 38 1785-1791. [Pg.191]

Adamietz et al. I" 106] treated Ehrlich ascites tumor cells, cultured in vitro, with bromelain. When exposure to bromelain was started at the time of cell plating, there was a temporary block of DNA synthesis, followed by a growth acceleration 48 hours Inlet Tumor cells already ad an ted to the substratum and... [Pg.146]

I. A. Adamietz, F. Kurfuist, U. Muller, K. Renner, and M. Rimpler. Growth acceleration of Ehrlich ascites tumor cells treated by proteinase in vitro. Eur, J. Cancer din. [Pg.152]

Partial inhibition of glycolysis by saturated fatty acids has been observed in Ehrlich ascites tumor cells. Palmitate and acetate decreased glutamate formation from glutamine (the first step in glutaminolysis) in this cell line, suggesting the possible role of fatty acids as an alternative energy source (Butler et al., 1999). [Pg.94]


See other pages where Ascites tumor cells is mentioned: [Pg.13]    [Pg.451]    [Pg.91]    [Pg.116]    [Pg.266]    [Pg.281]    [Pg.312]    [Pg.313]    [Pg.67]    [Pg.68]    [Pg.198]    [Pg.568]   
See also in sourсe #XX -- [ Pg.365 , Pg.367 ]




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